Glaucoma is an eye disease which is characterized by an increase of intraocular pressure. The increase of the pressure is caused by either a decreased aqueous outflow through Schlemm's canal or an abnormally increased secretion of aqueous humor. The mechanism for onset of glaucoma has not yet been sufficiently clarified. Conventional therapeutics consist of administration of pilocarpin, epinephrine, adrenergic beta-blocker, and the like. However, continuous use of adrenergic beta-blocker results in weakening in its action. In severe cases, surgical operations have been often conducted to decrease intraocular pressure. It is also known that among prostaglandin(PG)s, prostaglandins D.sub.3, E.sub.1, E.sub.2, E.sub.3, F.sub.2.alpha. and F.sub.2.alpha. derivatives show the activity of reducing intraocular pressure. (Chiryo 68, 1207-1213 (1986), Invest. Ophthalmol. Vis. Sci. Vol. 22, p. 588 (1982), 26, 1178-1182 (1985), Exp. Eye Res. 38, 181-194 (1984) and USP 4599353). Some of these prostaglandins, however, have a tendency to cause inflammational reactions. Furthermore, E and F type PGs incur a transient rise in intraocular pressure (IOP) before IOP reduction when administered in higher dose, which may aggravate the disease condition. Therefore, these PGs cannot be said to be appropriate for treatment of glaucoma.
In the course of the study on the pharmacological activity of prostaglandin D.sub.2 -active substance, the present inventors have found that the prostaglandin D.sub.2 -active substance can reduce the IOP without being accompanied by the transient rise in IOP.
The action of PGD.sub.2 per se on IOP has been reported in two articles. In the first article (Invest. Opthalmol. Vis. Sci. 23, 383-392, 1982), it was reported that PGD.sub.2 showed IOP raising activity in rabbits. In the second article (Exp. Eye Res. 38, 181-194, 1984, corresponding to U.S. Pat. No. 4,599,353) which deals mainly with PGF.sub.2.alpha. and its derivatives, PGD.sub.2 was administered to cats but the obtained result was not analyzed. In addition, according to the present inventors' analysis, the said data (-2.+-.0.8 mmHg, n=6) was not significant by Student's t-test indicating that PGD.sub.2 was not effective in that experiment. The reason why PGD.sub.2, contrary to the present inventors' finding, raised IOP or was ineffective on IOP in the experiments of the previous workers is not sufficiently clear. However, one of the causes may be attributed to the fact that the experimental animals used therein were, in our assumption, normal or lower IOP animals, in view of the present invention's finding that PGD.sub.2 does not reduce IOP of the normal or lower IOP rabbits. The present inventors, in contrast to the previous workers, used high IOP animals selected from the available rabbits and discovered that PGD.sub.2 has a reducing activity on IOP in such animals. Advantageously, PGD.sub. 2 has been found by the present inventors to cause no side effect such as hyperemia and flare which were observed on administration of PGE.sub.2, PGF.sub.2.alpha. and PGF.sub.2.alpha. derivatives. Furthermore, the present inventors also confirmed the above mentioned activity of PGD.sub.2 in human subjects.